Alcohol, diet, and experimental hepatic injury

Abstract

The concept of the prevention of fatty livers and cirrhosis by lipotropic factors and protein led to the notion that the latter might also be capable of affording protection against similar liver damage frequently seen in alcoholic man. The relevant literature, which had been published before the first investigations in this area were undertaken in Professor Best's department in 1949, is briefly cited. Developments in this field then utilized three approaches: experiments in which alcohol when administered in the drinking water supplied 27% of calories (Best), experiments with a completely fluid diet which supplied 36% of calories as alcohol (Lieber), and experiments in which an ethanol–sucrose mixture (Porta) in place of drinking water supplied 40–60% of calories as alcohol, with the remainder provided by semisynthetic diets. Most of the results obtained from these investigations did not support the concept of a direct hepatotoxic action of alcohol. Finally, evidence is presented that alcohol did not prevent regression of established cirrhosis in rats if they were treated by a "super diet" which contained abundant lipotropes and protein. Mallory bodies (alcoholic hyaline) formed in liver cells of alcohol-fed rats if basal diets were inadequate; the same structures appeared in rats fed certain other inadequate diets even without alcohol, and their development was prevented in rats consuming large amounts of alcohol if the basal diets were suitably fortified. The mitochondrial nature of these bodies was demonstrated. It is concluded that even large intakes of alcohol for weeks or months by rats do not injure their livers if the accompanying diet is suitably designed.